Free radicals, oxidative stress and importance of antioxidants in ...

Free radicals, oxidative stress and importance of antioxidants in ...


J M e d A l l i e d S c i 2 0 1 1 ; 1 ( 2 ) : 53- 60

w w w . j m a s . i n

P r i n t I S S N : 2 2 3 1 1696 O n l i n e I S S N : 2231 1 7 0 X

Journal of

M e d i cal &

Allied Sciences

Free radicals, oxidative stress and importance of

antioxidants in human health

Amit Kunwar and K.I. Priyadarsini

Radiation and Photochemistry Division,

Bhabha Atomic Research Centre, Trombay, Mumbai-400085, India.

Article history: Abstract

Received 13 March 2011

Revised 04 May 2011

Accepted 14 June 2011

Early online 01 July 2011

Print 31 July 2011

Corresponding author

Amit Kunwar

Radiation and Photochemistry Division,

Bhabha Atomic Research Centre,

Mumbai-400085, India.

Phone: +91 22 25595399

Fax: +91 22 25505151


eactive oxygen species (ROS) is a collective

term used for a group of oxidants, which are

either free radicals or molecular species capable

of generating free radicals. Intracellular generation

of ROS mainly comprises superoxide (O2 − )

radicals and nitric oxide (NO ) radicals. Under normal

physiologic conditions, nearly 2% of the oxygen

consumed by the body is converted into O2 −

through mitochondrial respiration, phagocytosis,

etc 1 . ROS percentage increases during infections,

exercise, exposure to pollutants, UV light, ionizing

radiation, etc. NO , is an endothelial relaxing factor

and neurotransmitter, produced through nitric oxide

synthase enzymes. NO and O2 − R

radicals, are converted

to powerful oxidizing radicals like hydroxyl

Reactive oxygen species (ROS) is a collective term used for oxygen

containing free radicals, depending on their reactivity and oxidizing

ability. ROS participate in a variety of chemical reactions with biomolecules

leading to a pathological condition known as oxidative

stress. Antioxidants are employed to protect biomolecules from the

damaging effects of such ROS. In the beginning, antioxidant research

was mainly aimed at understanding free radical reactions of

ROS with antioxidants employing biochemical assays and kinetic

methods. Later on, studies began to be directed to monitor the ability

of anti-oxidants to modulate cellular signaling proteins like receptors,

secondary messengers, transcription factors, etc. Of late several

studies have indicated that antioxidants can also have deleterious

effects on human health depending on dosage and bioavailability.

It is therefore, necessary to validate the utility of antioxidants

in improvement of human health in order to take full advantage

of their therapeutic potential.

Key words: Reactive oxygen species, oxidative stress, antioxidant


© 2011 Deccan College of Medical Sciences. All rights reserved.

radical ( OH), alkoxy radicals (RO ), peroxyl radicals

(ROO ), singlet oxygen ( 1 O2) by complex transformation

reactions. Some of the radical species are

converted to molecular oxidants like hydrogen peroxide

(H2O2), peroxynitrite (ONOO ), hypochlorous

acid (HOCl). Sometimes these molecular species

act as source of ROS.

For example, H2O2 is converted to OH radicals by

Fenton reaction and HOCl through its reaction with

H2O2 can be converted to 1 O2. ONOO at physiological

concentrations of carbon dioxide becomes a

source of carbonate radical anion (CO3 ) 1 . The various

pathways involved in the generation of ROS are

given in fig 1.


Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health

ROS in normal physiology

Typically, low concentration of ROS is essential for

normal physiological functions like gene expression,

cellular growth and defense against infection. Sometimes

they also act as the stimulating agents for biochemical

processes within the cell 2 . ROS exert their

effects through the reversible oxidation of active

sites in transcription factors such as nuclear factorkappa

B (NF-kB) and activator protein-1 (AP-1) leading

to gene expression and cell growth 3 . ROS can

also cause indirect induction of transcription factors

by activating signal transduction pathways 3 . One

example of signal transduction molecules activated

by ROS is the mitogen activated protein kinases

(MAPKs). ROS also appear to serve as secondary

messengers in many developmental stages. For

example, in sea urchins ROS levels are elevated

during fertilization. Similarly prenatal and embryonic

development in mammals has also been suggested

to be regulated by ROS 3 . Apart from these; ROS

also participate in the biosynthesis of molecules

such as thyroxin, prostaglandin that accelerate developmental

processes. It is noteworthy that in thyroid

cells, regulation of H2O2 concentration is critical

for thyroxine synthesis, as it is needed to catalyze

the binding of iodine atoms to thyroglobulin 3 . Finally

ROS are also used by the immune system. For example,

ROS have been shown to trigger proliferation

of T cells through NF-кB activation. Macrophages

and neutrophils generate ROS in order to kill the

bacteria that they engulf by phagocytosis. Furthermore,

tumor necrosis factor (TNF-α) mediates the

cytotoxicity of tumor and virus infected cells through

ROS generation and induction of apoptosis 2,3 .

Fig 1. Production of free radicals via different routes

ROS induced oxidative damages

Depending upon their nature, ROS (for e.g. OH radicals)

reactions with biomolecules such as lipid, protein

and DNA, produce different types of secondary

radicals like lipid radicals, sugar and base derived

radicals, amino acid radicals and thiyl radicals.

These radicals in presence of oxygen are converted

to peroxyl radicals. Peroxyl radicals are critical in

biosystems, as they often induce chain reactions 1 .

The biological implications of such reactions depends

on several factors like site of generation, nature

of the substrate, activation of repair mechanisms,

redox status among many others 4 .

For example, cellular membranes are vulnerable to

the oxidation by ROS due to the presence of high

concentration of unsaturated fatty acids in their lipid

components. ROS reactions with membrane lipids

cause lipid peroxidation, resulting in formation of

lipid hydroperoxide (LOOH) which can further decompose

to an aldehyde such as malonaldehyde, 4hydroxy

nonenal (4-HNE) or form cyclic endoperoxide,

isoprotans, and hydrocarbons. The consequences

of lipid peroxidation are cross linking of

membrane proteins, change in membrane fluidity

and formation of lipid-protein, lipid-DNA adduct

which may be detrimental to the functioning of the

cell 5 .

Proteins can undergo direct and indirect damage

following interaction with ROS resulting in to peroxidation,

changes in their tertiary structure, proteolytic

degradation, protein-protein cross linkages and

fragmentation 5 . The side chains of all amino acid

residues of proteins, in particular tryptophan, cyste-

J Med Allied Sci 2011; 1(2) 54

Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health

ine and methionine residues are susceptible to oxidation

by ROS. Protein oxidation products are usually

carbonyls such as aldehydes and ketones.

Although DNA is a stable, well-protected molecule,

ROS can interact with it and cause several types of

damage such as modification of DNA bases, single

and double strand DNA breaks, loss of purines (apurinic

sites), damage to the deoxyribose sugar, DNAprotein

cross-linkage and damage to the DNA repair

system 5 . Not all ROS can cause DNA damage and

OH radical is one of the potential inducers of DNA

damage. A variety of adducts are formed on reaction

of OH radical with DNA. The OH radical can attack

purine and pyrimidine bases to form OH radical adducts,

which are both oxidizing and reducing in nature.

This induces base modifications and sometimes

release of bases. Some of the important base

modifications include 8-hydroxydeoxyguanosine (8-

OHdG), 8 (or 4-, 5-)-hydroxyadenine, thymine peroxide,

thymine glycols and 5-(hydroxymethyl) uracyl 5 .

Free radicals can also attack the sugar moiety,

which can produce sugar peroxyl radicals and subsequently

inducing strand brakeage. The consequence

of DNA damage is the modification of genetic

material resulting in to cell death, mutagenesis,

carcinogenesis and ageing.

Antioxidants and natural defense from ROS induced


Uncontrolled generation of ROS can lead to their

accumulation causing oxidative stress in the cells.

Therefore, cells have evolved defense mechanisms

for protection against ROS mediated oxidative damage.

These include antioxidant defenses to keep a

check on the generation of ROS. An antioxidant is a

substance that is present at low concentrations and

significantly delays or prevents oxidation of the oxidizable

substrate 6 . Antioxidants are effective because

they can donate their own electrons to ROS

and thereby neutralizing the adverse effects of the

latter. In general, an antioxidant in the body may

work at three different levels: (a) prevention - keeping

formation of reactive species to a minimum e.g.

desferrioxamine (b) interception - scavenging reactive

species either by using catalytic and noncatalytic

molecules e.g. ascorbic acid, alphatocopherol

and (c) repair - repairing damaged target

molecules e.g. glutathione 6 . The antioxidant systems

are classified into two major groups, enzymatic antioxidants

and non enzymatic antioxidants. Enzymatic

antioxidants present in the body include superoxide

dismutase (SOD), catalase and glutathione peroxidase

(GPx) that act as body’s first line of defense

against ROS by catalyzing their conversion to less

reactive or inert species (Fig 2) 7 .

J Med Allied Sci 2011; 1(2)

Fig 2. Removal of different reactive oxygen species by antioxidant


Several low molecular weight molecules present

inside the cell provide secondary defense against

free radicals. A few examples of such molecules

include glutathione (GSH), α-tocopherol, ascorbate,

bilirubin, etc 6 . These agents either scavenge the

ROS directly or prevent the production of ROS

through sequestration of redox active metals like

iron and copper.

Redox state and oxidative stress

All forms of life maintain a steady state concentration

of ROS determined by the balance between

their rates of production and their rates of removal

by various antioxidants. Thus each cell is characterized

by a particular concentration of reducing species

like GSH, NADH, FADH, etc. stored in many

cellular constituents which determines the redox

state of a cell 6 . By definition redox state is the total

reduction potential or the reducing capacity of all the

redox couples such as GSSG/2GSH, NAD+/NADH,

Asc •− /AcsH − , etc found in biological fluids, organelles,

cells or tissues 8 . Redox state not only describes

the state of a redox pair, but also the redox

environment of a cell. Under normal conditions, the

redox state of a biological system is maintained towards

more negative redox potential values. However,

with increase in ROS generation or decrease

in antioxidant protection within cells, it is shifted towards

less negative values resulting in the oxidizing

environment (Fig 3). This shift from reducing status

to oxidizing status is referred as oxidative stress 6,8 .

During elevated oxidative stress, there is loss of mitochondrial

functions, which results in to ATP depletion

and necrotic cell death, while moderate oxidation

can trigger apoptosis. There are a few recent

reports have shown evidence that the induction of

apoptosis or necrosis during oxidative stress is actually

determined by the redox state of cell 8 . For example

it has been reported that an increase in reduction

potential of +72 mV in HL-60 cells (i.e., from

-239 ± 6 to -167 ± 9 mV) or an increase of +65 mV

in murine hybridoma cells (i.e., from -235 ± 5 to -170


Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health

± 8 mV) would cause induction of apoptosis 8 . Oxidative

stress has been implicated in a number of human

diseases like cancer, atherosclerosis, diabetics,

neurological diseases such as Alzheimer's disease,

Parkinson's disease, etc. as well as in the ageing


Fig 3. Balance between oxidant and antioxidant defines oxidative


Antioxidant supplementation

Although cells are equipped with an impressive repertoire

of antioxidant enzymes as well as small antioxidant

molecules, these agents may not be sufficient

enough to normalize the redox status during

oxidative stress 9 . Under such conditions supplementation

with exogenous antioxidants is required to

restore the redox homeostasis in cells. Recent epidemiological

studies have shown an inverse correlation

between the levels of established antioxidants

(vitamin E and C) / phytonutrients present in tissue /

blood samples and cardiovascular disease, cancer

and with mortality due to these diseases 10-12 . Since

several plant products are rich in antioxidants and

micronutrients, it is likely that dietary antioxidant

supplementation protects against the oxidative

stress mediated disease development. Therefore, to

maintain optimal body function, antioxidant supplementation

has become an increasingly popular practice.

Researchers are now attempting to develop

new antioxidants either of natural or synthetic origin.

Natural products as antioxidants

A variety of dietary plants including grams, legumes,

fruits, vegetables, tea, wine etc. contain antioxidants.

The prophylactic properties of dietary plants

have been attributed to the antioxidants / polyphenols

present in them. Polyphenols with over 8000

structural variants are secondary metabolites of

J Med Allied Sci 2011; 1(2)

plants and represent a huge gamut of substances

having aromatic ring(s) bearing one or more hydroxyl

moieties 13 . Polyphenols are effective ROS scavengers

and metal chelators due to the presence of

multiple hydroxyl groups. Examples of polyphenolic

natural antioxidants derived from plant sources include

vitamin E, flavonoids, cinnamic acid derivatives,

curcumin, caffeine, catechins, gallic acid derivatives,

salicylic acid derivatives, chlorogenic acid,

resveratrol, folate, anthocyanins and tannins 13 . Apart

from polyphenols there are also some plant derived

non-phenolic secondary metabolites such as melatonin,

carotenoids, retinal, thiols, jasmonic acid, eicosapentaenoic

acid, ascopyrones and allicin that

show excellent antioxidant activity 14,15 . Vitamin C,

the water soluble natural vitamin, plays a crucial role

in regenerating lipid soluble antioxidants like vitamin

E 6 . Both vitamin E and C are used as standards for

evaluating the antioxidant capacity of new molecules

6 . As an example, the antioxidant activity of

curcumin has been discussed in some detail in the

following section.

Curcumin a well-known natural antioxidant

Curcumin is a yellow pigment, the major constituent

of turmeric. It is a diferuloyl methane having an unsaturated

-diketone, and phenolic groups. It exhibits

a variety of pharmacological properties such as

anti-inflammatory, anti-carcinogenic, anti-microbial,

neuro-protective,cardio-protective,thrombo suppressive

and anti-diabetic actions 16,17 . The compound is

considered as a potent anti-cancer agent and is currently

being evaluated in different stages of clinical

trials against a variety of cancers 16 .

Curcumin is also a potent antioxidant. Studies from

our laboratory as well as others have shown it to be

an excellent scavenger of ROS such as O2 − radicals,

lipid peroxyl radicals, OH radicals and nitrogen

dioxide radicals, whose production is implicated in

the induction of oxidative stress 18,19 . Its free radical

scavenging ability is comparable to well known antioxidants

like vitamins C and E 19 . It has been shown

to inhibit lipid peroxidation in a variety of in vitro

models such as rat brain homogenates, rat liver microsomes,

erythrocytes, liposomes, and macrophages,

where peroxidation is induced by Fenton

reagent, H2O2, radiation and 2,2-azo-bis(2amidinopropane)

hydrochloride (AAPH) 19 . It has also

been reported to inhibit singlet oxygen-stimulated

DNA cleavage in plasmid pBR322 DNA, H2O2 and

AAPH induced hemolysis of erythrocytes 19,20 . In epithelial

cells, curcumin has been shown to increase

GSH levels which, in turn lead to lowered ROS production

21 . It also mediates its antioxidative effects by

elevating the levels of phase II enzymes such as


Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health

NAD(P)H:quinone reductase (QR) and antioxidant

enzymes like SOD, GPx and hemeoxygenase

(HO) 21,22 . For example, our previous study have

found that curcumin induces the expression of SOD,

GPx and HO-1 in RAW 264.7 (murine macrophage)

cells contributing to its antioxidant effects 22 . Similarly,

the in vitro incubation of bovine aortic endothelial

cells and human proximal renal tubular cells with

curcumin has been reported to result in dose and

time dependent increase of HO-1 mRNA, protein

expression and enzymatic activity 23 . The postulated

mechanism for these actions involves the activation

of PKC pathways and antioxidant response element

(ARE) mediated transcriptional induction. Curcumin

has also been shown to inhibit oxidative damage in

different animal models. For example, it inhibited

lipid degradation and decreased ischemia-induced

biochemical changes in heart in the feline model. In

a focal cerebral ischemia model of rats, it offered

significant neuroprotection through inhibition of lipid

peroxidation, increase in endogenous antioxidant

defense enzymes and reduction in peroxynitrite formation

24 . Further, studies on the mechanistic aspects

of antioxidant activity revealed that phenolic

hydroxyl groups of curcumin play a significant role in

its diverse antioxidant activity 25 . Some reports suggested

that both hydroxyl and diketone groups exert

antioxidant properties. The phenolic hydroxyl groups

give ROS scavenging ability and the diketone structure

is considered to be responsible for its ability to

bind to metals. The ability of curcumin to act as an

antioxidant in the presence of metals arises mainly

by preventing the Fenton chemistry within cells

through chelation of free metal ions such as Cu +2 ,

Fe +2 , etc 26 . There are some reports which indicate

that stable metal complexes of curcumin exhibit

higher antioxidant activity as compared to native

curcumin molecule. The manganese complexes of

curcumin were found to show greater SOD activity,

hydroxyl radical scavenging activity, and nitric oxide

radical scavenging activity than the parent molecules

27 . Similarly, our group has reported that copper

complex of curcumin also exhibits antioxidant,

superoxide-scavenging and SOD enzyme mimicking

activities superior to those of curcumin itself 28 .

These copper curcumin complexes were found better

than curcumin in preventing the γ-radiation induced

oxidative stress in splenic lymphocytes. The

associated mechanisms responsible for above effects

were identified as activation of cytoprotective

signaling components like protein kinase C delta

(PKC) and nuclear factor-B (NF--B) in temporally

relevant manner 29 . Thus, curcumin exhibits a variety

of antioxidant effects and appears to have a significant

potential in the treatment of multiple diseases

that are mediated through oxidative stress.

J Med Allied Sci 2011; 1(2)

Interestingly, reports are now appearing about apparently

contradictory pro-oxidative effects of curcumin.

For example, curcumin induced DNA fragmentation

and base damage in the presence of copper

and isozymes of cytochrome p450 (CYP) that

are present in lung, lymph, liver, and skin 30 . The authors

hypothesized that the damage was the result

of CYP-catalyzed O-demethylation of curcumin,

leading to the formation of an O-demethyl curcumin

radical, which, in the presence of copper, formed a

DNA-damaging Cu(I)-hydroperoxo complex. DNA

damage was attenuated when concentrations of

curcumin exceeded those of copper, presumably

due to the chelation of copper by curcumin. Copper

dependent formation of 8-hydroxy-deoxyguanosine

in response to curcumin was also reported (Yoshino

et al., 2004) and linked to apoptotic cell death in

HL60 cells 31 . Similarly, curcumin-mediated DNA

damage was also reported in mouse lymphocytes. In

agreement with these reports we also observed that

although curcumin inhibited that AAPH induced lipid

peroxidation and hemolysis in erythrocytes, it could

not prevent the leakage of K + ions. Rather, curcumin

itself induced K + ion release and GSH depletion at

higher concentration suggesting its pro-oxidant nature

20 . Further, our group has reported that curcumin

induced the ROS generation and GSH depletion in

RAW 264.7 cells in a concentration and time dependant

manner 22 . Of late, several reports have

emerged demonstrating pro-oxidative nature of curcumin,

in view of its ability to promote oxidative

stress in transformed cells in culture. These effects

have been correlated with enhanced ROS production,

alteration of the cellular redox homeostasis

(e.g., the depletion of glutathione), and disruption of

the mitochondrial functions e.g., dissipation of mitochondrial

inner transmembrane potential 32-35 . The

enhancement of oxidative stress by curcumin in

transformed cells ultimately results in mitochondrialmediated

apoptosis, and this has been considered

as one of the mechanisms responsible for the anticancer

activity of curcumin 32-35 . The mechanism by

which curcumin mediates its pro-oxidant effects is

not completely understood. However, some reports

suggest that curcumin irreversibly binds to mitochondrial

thioredoxin reductase, and modifies its

activity in to NADPH oxidase through alkylation of

cysteine residue present in the catalytically active

site of the enzyme 35 . This leads to the production of

ROS, which according to few others is due to the

α,β-unsaturated carbonyl moiety of curcumin 19 . The

pro-oxidant property is also believed to be due to the

generation of phenoxyl radicals of curcumin by

heme peroxidase-H2O2 system. These phenoxyl

radicals could be repaired by cellular GSH or NADH.

In this process, the resulting GS radical forms


Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health

GSSG radical and this may further reduce O2 to

form O2 radical leading to elevated ROS levels 36 .

In short, all these published reports support that curcumin

may switch from antioxidant to pro-oxidant

depending on cell type, redox environment and dosage.

A few reports also suggest that curcumin acts

as an antioxidant in normal cells while showing preferable

pro-oxidant behavior in tumor cells. It is this

differential property of curcumin, which makes it a

potent anti-tumor agent. The chemical structure of

curcumin and its reported antioxidant and prooxidant

mechanisms has been shown in fig 4.

Synthetic compounds as antioxidants

The use of synthetic compounds possessing antioxidant

activity for the preservation of cosmetic,

pharmaceutical and food products has been a common

practice. The most commonly used synthetic

antioxidants in the food industry are butylated 4hydroxytoluene

(BHT) and butylated 4hydroxyanisole

(BHA) 37 . However, the use of synthetic

antioxidants in the health industry has been

fraught with concerns about the toxicity associated

with synthetic compounds 16 . There are numerous

reports indicating that polyphenols which are the

major constituent of most of the natural antioxidants

are poorly bio-absorbed and the concentrations

achieved in the target tissues are sub-therapeutic in

vitro 38 . These findings have shifted the attention of

researches towards the development of synthetic,

water soluble, stable and nontoxic compounds with

potent antioxidant activity and therapeutic application.

Many different antioxidants and antioxidant

compositions have been developed over the years

based on their mechanism of action.

One group of such antioxidants includes molecules

that prevent the production of ROS through metal

ions sequestration, free radical scavenging or by

inhibiting the ROS producing enzymes. For example,

desferrioxamine an iron chelator have been

tested for preventing ROS formation in a myocardial

stunning model system following hemorrhagic and

endotoxic shock 39 . The allopurinol and other pyrazolopyrimidines,

which are inhibitors of xanthine oxidase,

have also been tested under similar disease

model system and have been found to be very effective.

Several congeners of GSH have been used in

various animal models to attenuate ROS induced

injury. For example, N-2-mercaptopropionylglycine

has been found to confer protective effects in a canine

model of myocardial ischemia and reperfusion

and N-acetylcysteine (NAC) has been used to treat

endotoxin toxicity in sheep. Dimethyl thiourea

(DMTU) and butyl-phenylnitrone (BPN) are believed

to scavenge hydroxyl radical, and have been shown

J Med Allied Sci 2011; 1(2)

to reduce ischemia reperfusion injury in rat myocardium

and in rabbits 40 .

Another important group of synthetic antioxidants

includes molecules that act as antioxidant enzyme

mimic and catalytically remove the ROS. For example,

the complex formed between the chelator, desferroxamine

and manganese possesses SOD activity

and has shown some activity in biological models,

but the instability of the metal ligand complex apparently

precludes its pharmaceutical use. Porphyrinmanganese

and curcumin-transition metal complexes

have also shown SOD activity and are under development

as SOD mimetic drugs 27 . Ebselen an organoselenium

compound exhibits GPx activity and

has been tested in clinic as anti-inflammatory drug 41 .

Recently our group has also been engaged in the

development of aliphatic water-soluble selenium

compounds as antioxidants. One such compound

diseledipropionic acid showed significant antioxidant

activity and potent in vivo radioprotection against

exposure to lethal dose of γ-radiation 42 .

Based on these studies, it is clear that a need exists

for antioxidant agents, which are efficient in removing

ROS, inexpensive to manufacture, stable, and

possess advantageous pharmacokinetic properties,

such as the ability to cross the blood-brain barrier

and penetrate tissues. Such versatile antioxidants

would find use as pharmaceuticals and possibly as


Limitations of antioxidant supplementation

The primary concern regarding antioxidant supplementation

is their potentially deleterious effects on

ROS production (pro-oxidant action) especially when

precise modulation of ROS levels are needed to allow

normal cell function 43 . In fact, some negative

effects of antioxidants when used in dietary supplements

(flavanoids, carotenoids, vitamin C and synthetic

compounds) have emerged in the last few

decades 11,12,44 . Mechanistic investigation has revealed

that antioxidants may exhibit pro-oxidant activity

depending on the specific set of conditions. Of

particular importance are their dosage, redox conditions

and also the presence of free transition metals

in cellular milieu 36,44 . For example, ascorbate, a wellknown

antioxidant in the presence of high concentration

of ferric iron is a potent mediator of lipid peroxidation.

Recent studies suggest that ascorbate

sometimes increases DNA damage in humans. Similarly

β-carotene also can behave as a pro-oxidant

in the lungs of smokers. Of note, natural antioxidant

compounds have relatively poor bioavailability. It is

therefore necessary to take into cognizance the bioavailability

and differential activities of natural and

synthetic antioxidant compounds before considering


Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health

J Med Allied Sci 2011; 1(2)

Fig 4. Important factors controlling the antioxidant and pro-oxidant activities of curcumin

them as therapeutic or pharmacological agents.


In this regard it is worth mentioning that at present

several natural as well as synthetic compounds are

available in the market as antioxidant supplements

in different formulations like capsules, tablets, etc.

with a direction to be consumed under specific diseased

condition. However, as a caution it is advised

to undertake the consumption of such supplements

only under a strict medical supervision in order to

avoid the dosage related negative effects.


The authors are also grateful to Dr. S.K. Sarkar,

Head, RPC Division and Dr. T. Mukherjee, Director,

Chemistry Group, BARC for encouragement.

Conflict of interest: None


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